ライフサイエンスコーパス: acetyl-CoA

1 Coenzyme A (CoA) and acetyl-coenzyme A (acetyl-CoA) are ubiquitous cellular molecules, which med

2 the related metabolism of acetyl-coenzyme A (acetyl-CoA) confer numerous metabolic functions, includi

3 Acetyl coenzyme A (acetyl-CoA) generated from glucose and acetate uptake is

4 atalyze the hydrolysis of acetyl-Coenzyme A (acetyl-CoA) in the absence of an arylamine substrate usi

5 Metabolic production of acetyl coenzyme A (acetyl-CoA) is linked to histone acetylation and gene re

6 , suggesting an increased acetyl coenzyme A (acetyl-CoA) load.

7 homeostasis by regulating acetyl-coenzyme A (acetyl-CoA) metabolism.

8 on source utilization for acetyl coenzyme A (acetyl-CoA) production and gluconeogenesis.

9 The metabolite acetyl-coenzyme A (acetyl-CoA) serves as an essential element for a wide ra

10 oxylate is condensed with acetyl coenzyme A (acetyl-CoA) to give malate, which undergoes two oxidativ

11 LY) synthesizes cytosolic acetyl coenzyme A (acetyl-CoA), a fundamental cellular building block.

12 ve to the availability of acetyl coenzyme A (acetyl-CoA), we investigated a role for metabolic regula

13 that A-485 competes with acetyl coenzyme A (acetyl-CoA).

14 biosynthesis of cytosolic acetyl coenzyme A (acetyl-CoA, the two-carbon isoprenoid precursor) with a

15 nted by increasing FAO via deletion of ACC2 (acetyl-CoA-carboxylase 2) in phenylephrine-stimulated ca

16 c1(S/A) cells exhibit a reduction in acetate/acetyl-CoA availability along with elevated cellular lip

17 that artificial perturbation of the acetate/acetyl-CoA balance alters the acetyl-lysine occupancy of

18 ) protein levels in chicken liver, activated acetyl-CoA carboxylase (ACCalpha), and increased FASN, A

19 esulting structural features in AMP- and ADP-acetyl-CoA synthetase proteins in this study expand the

20 rates revealed the greatest activity against acetyl-CoA, and structure-guided mutagenesis of putative

21 inds prior to agmatine to generate an AgmNAT*acetyl-CoA*agmatine ternary complex prior to catalysis.

22 two models of AT-1 dysregulation and altered acetyl-CoA flux: AT-1(S113R/+) mice, a model of AT-1 hap

23 and fatty acid oxidation, activated the AMPK-acetyl-CoA carboxylase pathway, and promoted inefficient

24 M (S-adenosylmethionine) synthetases, and an acetyl-CoA synthetase.

25 sphate needed for the synthesis of ATP by an acetyl-CoA synthetase.

26 rted P. falciparum drug resistance genes, an acetyl-CoA transporter (pfact) and a UDP-galactose trans

27 Sphingosine kinase1 (SphK1) is an acetyl-CoA dependent acetyltransferase which acts on cyc

28 bolism mediated by the SREBP-SCD pathway, an acetyl-CoA carboxylase (ACC) and certain nuclear hormone

29 spite nutrient excess, induced both AMPK and acetyl-CoA carboxylase (ACC) phosphorylation.

30 the C terminus to facilitate CoA binding and acetyl-CoA production.

31 ural conformations in succinyl-CoA-bound and acetyl-CoA-bound forms.

32 -CoA, crotonyl-CoA, 3-hydroxybutyryl-CoA and acetyl-CoA as observable intermediates.

33 r identification and quantitation of CoA and acetyl-CoA ex vivo in tissue.

34 mRNA levels of fatty acid synthase (Fas) and acetyl-CoA carboxylase (Acc1).

35 mide adenine dinucleotide, reduced form) and acetyl-CoA levels.

36 ase (PFL) converting pyruvate to formate and acetyl-CoA.

37 nutrients including glucose, glutamine, and acetyl-CoA.

38 to serious metabolic diseases in humans, and acetyl-CoA carboxylase is a target for drug discovery in

39 esponded to AMP-activated protein kinase and acetyl-CoA carboxylase signaling.

40 s well as a protease subunit (clpP)-like and acetyl-CoA carboxylase subunit D (accD)-like open readin

41 included higher levels of neutral lipid and acetyl-CoA in WT tumors.

42 largely leave out how and why ATP, NADH, and acetyl-CoA (Figure 1 ) at the molecular level play such

43 called out three metabolites: ATP, NADH, and acetyl-CoA, as sentinel molecules whose accumulation rep

44 ate and coenzyme A (CoA) to oxaloacetate and acetyl-CoA(1-5).

45 he overexpression of genes encoding PEX7 and acetyl-CoA carboxylase further improved fatty alcohol pr

46 In biochemical production, pyruvate and acetyl-CoA are primary building blocks.

47 As pyruvate and acetyl-CoA play central roles in cellular metabolism, un

48 PKM2 directs the synthesis of pyruvate and acetyl-CoA, the latter of which is transported to mitoch

49 cose carbon flow via OAA-malate-pyruvate and acetyl-CoA-fatty acid pathways in TRCs.

50 ion, increased phosphorylation of raptor and acetyl-CoA carboxylase, and decreased phosphorylation of

51 proteins, alkyl hydroperoxide reductase and acetyl-CoA acetyltransferase, recognizing TPT were cruci

52 identify a circuit between AKT signaling and acetyl-CoA metabolism regulated via TCR signal strength

53 The expression of fatty acid synthase and acetyl-CoA carboxylase involved in de novo biosynthesis

54 growing appreciation that molecules such as acetyl-CoA act as a shared currency between metabolic fl

55 ural plasticity and establish a link between acetyl-CoA generation 'on-site' at chromatin for histone

56 -limiting enzyme of fatty acid biosynthesis, acetyl-CoA carboxylase 1 (ACC1), is O-GlcNAcylated and n

57 diauxic shift, along with expression of both acetyl-CoA synthetase genes ACS1 and ACS2 We conclude th

58 is produced from acetate by chromatin-bound acetyl-CoA synthetase 2 (ACSS2)(2).

59 tyl sphingosine (N-AS) is first generated by acetyl-CoA and sphingosine through SphK1.

60 oA biosynthesis and is feedback-inhibited by acetyl-CoA.

61 cid synthesis (FAS) is partially mediated by acetyl-CoA carboxylase (ACCase), the first committed ste

62 CLY) from mitochondria-derived citrate or by acetyl-CoA synthetase short-chain family member 2 (ACSS2

63 e allosteric inhibition of beta-oxidation by acetyl-CoA.

64 decreased flux of [U-(13)C]glucose to [(13)C]acetyl-CoA and M2 and M4 isotopomers of tricarboxylic ac

65 rotein transfers acetyl groups from [(14) C]-acetyl-CoA to oligogalacturonides.

66 inant HMGL35 is the active enzyme catalyzing acetyl-CoA and acetoacetate synthesis when incubated wit

67 he Taxol biosynthetic machinery and cellular acetyl-CoA of A. terreus have been completely restored u

68 ly visualize absolute concentrations of CoA, acetyl-CoA, and endogenous CoA-S-S-G along with redox co

69 However, its main role is to consume acetyl-CoA, which unlocks isocitrate dehydrogenase (IDH)

70 They convert acetyl-CoA to ethanol via an acetaldehyde intermediate d

71 alonate pathway in the peroxisome to convert acetyl-CoA to several commercially important monoterpene

72 enzyme in bacterial fermentation, converting acetyl-CoA to ethanol, via two consecutive catalytic rea

73 C2 action is controlling nuclear-cytoplasmic acetyl-CoA synthesis.

74 precursor for lipid biosynthesis, cytosolic acetyl CoA (Ac-CoA), is produced by ATP-citrate lyase (A

75 oA generating system provided by a cytosolic acetyl-CoA carboxylase, the mitochondrial AAE13 protein

76 Manipulation of alternative cytosolic acetyl-CoA pathways partially decoupled lipogenesis from

77 he citrate-malate shuttle supplies cytosolic acetyl-CoA and plastidic glycolysis and malic enzyme sup

78 deficiency markedly lowered total cytosolic acetyl-CoA levels, which led to decreased Raptor acetyla

79 ular acetate levels resulting from decreased acetyl-CoA synthetase activity.

80 source exhibited decreased growth, decreased acetyl-CoA, and increased intracellular acetate levels r

81 between decreased phosphorylation, decreased acetyl-CoA carboxylase Acc1 phosphorylation, and sterol

82 tically, the perturbations to AT-1-dependent acetyl-CoA flux result in global and specific changes in

83 by substituting for the depleted FAO-derived acetyl-CoA) or a nucleoside mix rescued the phenotype of

84 acetyl-CoA compensating when glucose-derived acetyl-CoA is limiting.

85 stone H4 acetylation, with glutamine-derived acetyl-CoA compensating when glucose-derived acetyl-CoA

86 t high heteroplasmy, mitochondrially derived acetyl-CoA levels decrease causing decreased histone H4

87 cetyl-CoA relative to beta-oxidation-derived acetyl-CoA, are suggested to impact on insulin-stimulate

88 These results identify peroxisome-derived acetyl-CoA as a key metabolic regulator of autophagy tha

89 oxylic acid cycle influx of pyruvate-derived acetyl-CoA relative to beta-oxidation-derived acetyl-CoA

90 However, pyruvate decarboxylation during acetyl-CoA formation limits the theoretical maximum carb

91 and inhibition of citrate synthase, elevated acetyl-CoA levels, and hyperacetylation of mitochondrial

92 Dichloroacetic acid treatment elevated acetyl-CoA levels, restored mTORC1 activation, inhibited

93 Mxr1p is a key regulator of ACS1 encoding acetyl-CoA synthetase in cells cultured in YPA.

94 ss is controlled by the rate-limiting enzyme acetyl-CoA carboxylase (ACC), an attractive but traditio

95 le including Acc1p, the rate-limiting enzyme acetyl-CoA carboxylase.

96 Here we show that the metabolic enzyme acetyl-CoA synthetase 2 (ACSS2) directly regulates histo

97 ssion measurements of key lipogenic enzymes [acetyl CoA carboxylase 1 (ACC1), fatty acid synthase (FA

98 On the other hand, the excess acetyl-CoA generated as a result of ACL induction provid

99 nthesis enzymes [fatty acid synthase (FASN), acetyl-CoA carboxylase (ACC), ATP citrate lyase (ACLY)].

100 s, potentially relevant to pathogen fitness, acetyl-CoA/propionyl-CoA intracellular balance and secon

101 ology (CSH) module, flanked by four flexible acetyl-CoA synthetase homology (ASH) domains; CoA is bou

102 first four characterized proteins: BEAT [for acetyl CoA:benzylalcohol acetyltransferase], AHCT [for a

103 the understanding of the molecular basis for acetyl-CoA synthesis by ACLY.

104 Pyruvate and butyrate competed for acetyl-CoA production, as evidenced by significant chang

105 rather than citrate lyase, is essential for acetyl-CoA synthesis in fission yeast.

106 e for the first time that CL is required for acetyl-CoA synthesis, which is decreased in CL-deficient

107 yltransferase protein and is responsible for acetyl-CoA synthetase acetylation.

108 tion of CO, CoA, and a methyl-cation to form acetyl-CoA at a unique Ni,Ni-[4Fe4S] cluster (the A-clus

109 lyzes the formation of N-acetylagmatine from acetyl-CoA and agmatine.

110 Its biosynthesis from acetyl-CoA is the primary target of the most commonly us

111 l enzymes that commonly produce ethanol from acetyl-CoA with acetaldehyde as intermediate and play a

112 .178), which transfers the acetyl group from acetyl-CoA to EctB-formed l-2,4-diaminobutyrate (DAB), y

113 talyzes the transfer of an acetyl group from acetyl-CoA to the sn-3 position of diacylglycerol to for

114 lyzing the transfer of an acetyl moiety from acetyl-CoA to the C-4 amino group of UDP-d-viosamine.

115 -limiting conditions, but how cells generate acetyl-CoA under starvation stress is less understood.

116 enzyme cleaves cytosolic citrate to generate acetyl-CoA, and is upregulated after consumption of carb

117 and NAD(+) and by SpxB and PDHc to generate acetyl-CoA.

118 silencing of hepatic ACSS2, which generates acetyl-CoA from acetate, potently suppresses the convers

119 sult, expression of the mSREBP1 target genes acetyl-CoA carboxylase and fatty-acid synthase was suppr

120 presses HGP is through reductions in hepatic acetyl CoA by suppression of lipolysis in white adipose

121 e HPA axis and ensuing reductions in hepatic acetyl CoA content as a common mechanism responsible for

122 Insulin's ability to suppress hepatic acetyl CoA, PC activity, and lipolysis was lost in high-

123 e adipose tissue (WAT) lipolysis and hepatic acetyl-CoA content, rates of hepatic glucose production,

124 he liver, which results in increased hepatic acetyl-CoA content, a potent activator of pyruvate carbo

125 he conversion of bolus fructose into hepatic acetyl-CoA and fatty acids.

126 ride lipase, intrahepatic lipolysis, hepatic acetyl-CoA content and pyruvate carboxylase flux, while

127 nase B-dependent manner, to regulate hepatic acetyl-CoA and cholesterol synthesis.

128 , the route from dietary fructose to hepatic acetyl-CoA and lipids remains unknown.

129 nts, expresses a multicomponent, heteromeric acetyl-CoA carboxylase (htACCase), which catalyzes the g

130 However, how acetyl-CoA is produced under nutritional stress is uncle

131 f target genes encoding proteins involved in acetyl CoA and pyruvate metabolism.

132 strength and that transient fluctuations in acetyl-CoA levels function in T cell fate decisions.

133 by which a cell responds to fluctuations in acetyl-CoA levels remain elusive.

134 via glutamate dehydrogenase and reduction in acetyl-CoA pools, which in turn induce autophagy and cel

135 tudy expand the ASKHA superfamily to include acetyl-CoA synthetase.

136 involved in fatty acid synthesis, including acetyl-CoA carboxylase, and three out of five putative t

137 In B cells, SCFAs increase acetyl-CoA and regulate metabolic sensors to increase ox

138 ion, elevating glucose uptake, and increased acetyl-CoA levels, leading to more ROS generation in hyp

139 Indeed, CR increased acetyl-CoA levels during the diauxic shift, along with e

140 utilization, Cpt1b(M-/-) mice have increased acetyl-CoA (14-fold) and NADH (2-fold), indicating metab

141 cose promotes HspQ acetylation by increasing acetyl-CoA amounts, thereby linking metabolism to proteo

142 P-1(32-36)amide activated AMPK and inhibited acetyl-CoA carboxylase, suggesting activation of fat met

143 AMPK phosphorylates and inhibits acetyl-CoA carboxylase (ACC), which catalyzes carboxylat

144 ther suggests that oxidation of intermediary acetyl-CoA to CO(2) occurs through the oxidative Wood-Lj

145 The metabolic intermediate acetyl-CoA links anabolic and catabolic processes and co

146 Intracellular acetyl-CoA concentrations are associated with nutrient a

147 The level of intracellular acetyl-CoA influx was reduced sequentially with the fung

148 of the nucleolus as an important hub linking acetyl-CoA fluctuations to cellular stress responses.

149 tein content of adipose triglyceride lipase, acetyl-CoA carboxylase 2 and AMP-activated protein kinas

150 t microbiota(9), and this supplies lipogenic acetyl-CoA independently of ACLY(10).

151 ation were observed with a HFD despite lower acetyl-CoA levels.

152 ]glucose or [1,2-(13)C2]palmitate) or/and M1 acetyl-CoA (e.g. [1-(13)C]octanoate).

153 or two labeled substrates, which generate M2 acetyl-CoA (e.g. [(13)C6]glucose or [1,2-(13)C2]palmitat

154 important metabolic regulator that maintains acetyl-CoA homeostasis by promoting functional crosstalk

155 atine using an ordered sequential mechanism; acetyl-CoA binds prior to agmatine to generate an AgmNAT

156 AMP-activated protein kinase (AMPK)-mediated acetyl-CoA synthetase 2 (ACSS2) phosphorylation at S659,

157 abeling rate ( 0.03 h(-1)) of key metabolite acetyl-CoA reached to P7 strain's metabolism limitation

158 ylation of histones relies on the metabolite acetyl-CoA, which is produced from acetate by chromatin-

159 report that binding of the lipid metabolites acetyl-CoA or propionyl-CoA to ICL2 induces a striking s

160 Mitochondrial acetyl-CoA acetyltransferase 1 (ACAT1) regulates pyruvat

161 n isotopic technique to assess mitochondrial acetyl-CoA turnover ( approximately citric acid flux) in

162 te oxidation and generation of mitochondrial acetyl-CoA, were used for metabolic intervention.

163 c environment," the hepatocyte diverted more acetyl-CoA away from lipogenesis toward ketogenesis and

164 several fatty acid synthesis genes, namely, acetyl-CoA carboxylase, fatty acid synthase, SREBP1c, ch

165 citrate synthase promotes increased nuclear acetyl-CoA levels, increased histone acetylation at the

166 A decrease in ACSS2 lowers nuclear acetyl-CoA levels, histone acetylation, and responsive e

167 eacetylation by increasing nucleocytoplasmic acetyl-CoA levels impairs Wnt3a-induced osteoblast diffe

168 egulates the availability of nucleocytosolic acetyl-CoA for protein acetylation and that AMPK activat

169 timizing the coordination of nucleocytosolic acetyl-CoA production with massive reorganization of the

170 (ACLY) is a major source of nucleocytosolic acetyl-CoA, a fundamental building block of carbon metab

171 etion and early pharmaceutical inhibition of acetyl CoA carboxylase 1, the rate limiting step of FAS,

172 n chronic infection, a specific inhibitor of acetyl CoA carboxylase 1, 5-(tetradecyloxy)-2-furoic aci

173 llular acetate and decreased accumulation of acetyl-CoA-derived intermediates of central metabolism.

174 tion in bacteria involves the acetylation of acetyl-CoA synthetase, whose activity must be tightly re

175 ode of activity as a competitive analogue of acetyl-CoA.

176 mitochondria, and although carboxylation of acetyl-CoA is the known mechanism for generating the dis

177 lase (ACC), which catalyzes carboxylation of acetyl-CoA to malonyl-CoA, the first and rate-limiting r

178 Nucleocytosolic concentration of acetyl-CoA affects histone acetylation and links metabol

179 cle, whereas the myocardial concentration of acetyl-CoA was significantly increased in end-stage hear

180 Thus, the spatial and temporal control of acetyl-CoA production by ACLY participates in the mechan

181 ation of ACC and decreases the conversion of acetyl-CoA to malonyl-CoA, leading to increased protein

182 in the HGSNAT gene leading to deficiency of acetyl-CoA: alpha-glucosaminide N-acetyltransferase invo

183 glycolytic genes and a significant delay of acetyl-CoA accumulation and reentry into growth from qui

184 The development of acetyl-CoA carboxylase (ACC) inhibitors for the treatmen

185 glucose uptake with consequent diversion of acetyl-CoA into ketogenesis.

186 atic steatosis, as well as the expression of acetyl-CoA carboxylase and fatty acid synthase.

187 ed for optimal PDH activation, generation of acetyl-CoA, and TCA cycle function, findings that link t

188 AMPK thus regulates homeostasis of acetyl-CoA, a key metabolite at the crossroads of metabo

189 The import of acetyl-CoA into the lumen of the endoplasmic reticulum (

190 fructose in a manner that is independent of acetyl-CoA metabolism.

191 ht be due to the reduction on main influx of acetyl-CoA, or downregulation of ribosome biogenesis pro

192 cell culture and mice via the inhibition of acetyl-CoA carboxylase 1 (ACC1), resulting in neuroprote

193 nergy-sensing enzyme AMPK, and inhibition of acetyl-CoA carboxylase and mammalian target of rapamycin

194 tissue and increased UCP-3 and inhibition of acetyl-CoA carboxylase in skeletal muscle, findings cons

195 reversible NADH-mediated interconversions of acetyl-CoA, acetaldehyde, and ethanol but seemed to be p

196 enesis in mice by liver-specific knockout of acetyl-CoA carboxylase (ACC) genes and treat the mice wi

197 tivities but, rather, decreases the level of acetyl-CoA in the nucleus.

198 mice consuming a HFD have reduced levels of acetyl-CoA and/or acetyl-CoA:CoA ratio in these tissues.

199 bacterial cell responds to lowered levels of acetyl-CoA by inducing RpoS, allowing reprogramming of E

200 s accompanied by decreased protein levels of acetyl-CoA carboxylase, a key regulator of both lipid ox

201 ased flux was secondary to greater levels of acetyl-CoA from metabolic reprogramming to beta oxidatio

202 CMS121 and J147 increased the levels of acetyl-CoA in cell culture and mice via the inhibition o

203 manipulate the nucleo-cytoplasmic levels of acetyl-CoA using clustered regularly interspaced short p

204 alter the redox state and cellular levels of acetyl-CoA, resulting in altered histone acetylation, ge

205 The majority of acetyl-CoA generated by PFL was used to regenerate NAD(+

206 The method was applied to measurements of acetyl-CoA turnover under different conditions (glucose

207 synthase homology domain in the mechanism of acetyl-CoA formation.

208 m was gathered from the labeling patterns of acetyl-CoA proxies, i.e. total acetyl-CoA, the acetyl mo

209 t cells and that required phosphorylation of acetyl-CoA carboxylase (ACC) 1 and/or ACC2 at the AMPK s

210 induced autophagy and the phosphorylation of acetyl-CoA carboxylase (ACC), whereas alone it could blo

211 n augmenting AMPK-induced phosphorylation of acetyl-CoA carboxylase and in activating the PI3K/AKT pa

212 roptosis to AMPK-mediated phosphorylation of acetyl-CoA carboxylase and polyunsaturated fatty acid bi

213 f microbial acetate feeds lipogenic pools of acetyl-CoA.

214 he liver(4-6), in which carbon precursors of acetyl-CoA are converted into fatty acids.

215 onstituting them in vitro in the presence of acetyl-CoA, UDP- N-acetylglucosamine, NADPH, and ATP, we

216 o up-regulated, leading to the production of acetyl-CoA, which can feed TAG accumulation upon exposur

217 ance for nuclear ACLY-mediated production of acetyl-CoA, which promotes histone acetylation, BRCA1 re

218 or cost-effective, large-scale production of acetyl-CoA-derived molecules.

219 atment increased ACC levels and the ratio of acetyl-CoA to free CoA in these animals, indicating incr

220 A sharp reduction of acetyl-CoA and ATP levels in NCTC cells indicated reduce

221 response to acetyl-CoA and the regulation of acetyl-CoA synthetase activity by the acetylation level.

222 ional and/or posttranslational regulation of acetyl-CoA synthetase and ADP-Glc pyrophosphorylase, and

223 The synthesis of acetyl-CoA depends primarily on the PDH-catalyzed conver

224 haea, catalyzing the reversible synthesis of acetyl-CoA from CO and a methyl group through a series o

225 adipose and liver, but the impact of diet on acetyl-CoA and histone acetylation in these tissues rema

226 HFD have reduced levels of acetyl-CoA and/or acetyl-CoA:CoA ratio in these tissues.

227 o the lipid biosynthetic precursors NADPH or acetyl-CoA.

228 y supplying additional pentanoate-originated acetyl-CoA for histone acetyltransferases, and by pentan

229 n the selective binding of succinyl-CoA over acetyl-CoA.

230 Comparison of the human PANK3.acetyl-CoA complex to the structures of PANK3 in four ca

231 tone acetylation turnover to locally produce acetyl-CoA for histone H3 acetylation in these regions a

232 thelial cells oxidize fatty acids to produce acetyl-CoA for epigenetic modifications critical to lymp

233 Acetate is utilized to produce acetyl-CoA without carbon loss or redox imbalance.

234 ion in the diabetic heart, with the produced acetyl-CoA channelled into the tricarboxylic acid cycle.

235 ATP citrate-lyase produces acetyl-CoA in the nucleus and cytosol and regulates hist

236 s additionally implicate mTORC2 in promoting acetyl-CoA synthesis from acetate through acetyl-CoA syn

237 nase, which results in reduction in pyruvate/acetyl-CoA conversion, mitochondrial reactive oxygen spe

238 By raising acetyl-CoA concentration ACL promotes H3K9/14 and H3K27

239 AMPK deletion reduced acetyl-CoA and histone acetylation, displacing BET prote

240 The ancient reductive acetyl-CoA pathway is employed by acetogenic bacteria to

241 sis to carbon fixation through the reductive acetyl-CoA [Wood-Ljungdahl pathway (WLP)], which was int

242 etate production as well as in the reductive acetyl-CoA pathway were detected in all four genomes inf

243 xidative decarboxylation steps to regenerate acetyl-CoA.

244 We also found that AT-1 activity regulates acetyl-CoA flux, causing epigenetic modulation of the hi

245 We find that TCR signaling regulates acetyl-CoA metabolism via AKT in murine CD4(+) T cells.

246 ty acid-responsive factor Oaf1 in regulating acetyl-CoA production in glucose grown cells.

247 We used the dexamethasone system to silence acetyl-CoA carboxylase gene and observed prolific root g

248 Besides the conventional carbon sources, acetyl-CoA has recently been shown to be generated from

249 regulatory element-binding protein [SREBP], acetyl-CoA carboxylase [ACC], peroxisome proliferator-ac

250 Acly in cultured adipocytes also suppressed acetyl-CoA and histone acetylation levels.

251 upplementation allows the cell to synthesize acetyl-CoA by an alternative, less favored pathway, in p

252 PDH synthesizes acetyl-CoA; acetate supplementation allows the cell to s

253 PDH bypass in the cytosol, which synthesizes acetyl-CoA from acetate.

254 d state of AMPK and of its downstream target acetyl-CoA carboxylase.

255 AMP-activated protein kinase and its target acetyl-CoA carboxylase.

256 velopment of novel ACLY modulators to target acetyl-CoA-dependent cellular processes for potential th

257 phloem-mobile systemic insecticide targeting acetyl-CoA carboxylase (ACC) of pest insects and mites u

258 -CoA and histone acetylation levels and that acetyl-CoA abundance correlates with acetylation of spec

259 titative omics analyses, we demonstrate that acetyl-CoA depletion alters the integrity of the nucleol

260 Our results also demonstrated that acetyl-CoA or acetyl-phosphate could acetylate MDH chemi

261 We show that acetyl-CoA synthase, rather than citrate lyase, is essen

262 Preclinical and clinical data suggest that acetyl-CoA carboxylase (ACC) inhibitors have the potenti

263 The acetyl-CoA product is crucial for the metabolism of fatt

264 The acetyl-CoA-dependent enzyme YvoF is a close relative of

265 central carbon metabolism and augmenting the acetyl-CoA pool.

266 Additional suppressor mutations in the acetyl-CoA binding site of pyruvate carboxylase (PycA) r

267 modomain (p.Arg53His) and two at or near the acetyl-CoA binding site (p.Cys369Ser and p.Ser413Ala).

268 of accD (the plastid-encoded subunit of the acetyl-CoA carboxylase, which catalyzes the first and ra

269 -bound p300 HAT complexes and shows that the acetyl-CoA binding site is stably formed in the absence

270 subset used in capsule production, while the acetyl-CoA generated by SpxB and PDHc was utilized prima

271 Time dependent studies showed that while the acetyl-CoA levels remain unaltered, CoA levels diminish

272 several histone lysines correlated with the acetyl-CoA: (iso)butyryl-CoA ratio in liver.

273 monstrated that GCBCs generate most of their acetyl-CoA and acetylcarnitine from FAs.

274 ng acetyl-CoA synthesis from acetate through acetyl-CoA synthetase 2 (ACSS2).

275 e as activated forms of acetate analogous to acetyl-CoA.

276 ynthesis) and eat it (degrade acyl chains to acetyl-CoA).

277 lyase (ACL), an enzyme converting citrate to acetyl-CoA, is highly induced in the kidney of overweigh

278 bolism of cyclohex-1,5-diene carboxyl-CoA to acetyl-CoA were in high abundance in S. aciditrophicus c

279 uted a decreased carbon flux from glucose to acetyl-CoA in the TAZ-KO cells to a ~50% decrease in pyr

280 nched-chain amino acid catabolism leading to acetyl-CoA production.

281 Acetate (metabolized to acetyl-CoA, thereby substituting for the depleted FAO-de

282 The acetaldehyde produced is oxidized to acetyl-CoA by a dehydrogenase, and the sulfite is reduce

283 By converting pyruvate to acetyl-CoA (AcCoA), the pyruvate dehydrogenase (PDH) com

284 O2 due to the decarboxylation of pyruvate to acetyl-CoA and limitations in the reducing power of the

285 ondrial matrix where it converts pyruvate to acetyl-CoA.

286 hich catalyzes the conversion of pyruvate to acetyl-CoA.

287 ltienzyme assembly that converts pyruvate to acetyl-CoA.

288 d PatZ-positive cooperativity in response to acetyl-CoA and the regulation of acetyl-CoA synthetase a

289 c catalytic activity and is not sensitive to acetyl-CoA activation, in contrast to other PC enzymes.

290 y glycine reductase to acetyl-P, and then to acetyl-CoA, which is condensed with another CO(2) to for

291 g patterns of acetyl-CoA proxies, i.e. total acetyl-CoA, the acetyl moiety of citrate, C-1 + 2 of bet

292 tose, pyruvate metabolism was shunted toward acetyl-CoA production.

293 phosphoryl transfers (ATP), acyl transfers (acetyl-CoA, carbamoyl-P), methyl transfers (SAM), prenyl

294 A1, a membrane transporter that translocates acetyl-CoA from the cytosol into the endoplasmic reticul

295 lum (ER) acetylation machinery, transporting acetyl-CoA from the cytosol into the ER lumen where acet

296 uctase (rPFOR), which incorporates CO2 using acetyl-CoA as a substrate and generates pyruvate, and py

297 h increased ketogenic/lipogenic activity via acetyl-CoA, 3-hydroybutyrate, and cholesterol metabolite

298 CoA from the cytosol into the ER lumen where acetyl-CoA serves as the acetyl-group donor for Nepsilon

299 ACLY with acetyl-CoA and oxaloacetate products shows the products

300 d in all species and catalyse reactions with acetyl-CoA or propionyl-CoA.